1 Capsaicin (Cap) enhanced the twitch response of the epididymal and prostatic portions of rat vas deferens induced by field stimulation at 0.1 Hz. The effect of Cap was reproducible and showed no desensitization. 2 Prazosin, and pretreatment with reserpine or Cap did not affect the potentiating effect of Cap, whereas pretreatment with 6-hydroxydopamine abolished the action of Cap. 3 Cap tended to attenuate the contractions induced by noradrenaline, tyramine and ATP. 4 Like Cap, substance K and substance P augmented the twitch response without causing desensitization, but their effects differed somewhat from that of Cap. Calcitonin gene-related peptide inhibited the twitch response. 5 These results suggest that Cap enhances a stimulation-induced, prazosin-resistant non-adrenergic twitch response of rat vas deferens through an as yet undefined prejunctional mechanism. This mechanism is possibly mediated by some peptide released in response to Cap from sensory neurones, which in turn acts on sympathetic nerves and increases stimulation-induced release of a mediator or cotransmitter responsible for the non-adrenergic twitch response. However, the possibility that Cap has a direct action on sympathetic nerves cannot be ruled out.

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5-Hydroxytryptamine (5-HT) slightly inhibited the twitch contractions of rat vas deferens caused by single pulse field stimulation at 0.1 Hz. The inhibitory effect of 5-HT was much less in the epididymal portion than in the prostatic portion of the vas deferens. Ketanserin potentiated the prejunctional inhibitory effect of 5-HT and attenuated its stimulatory effect. This potentiation was observable only in the epididymal portion, of the vas deferens. Cyproheptadine and mianserin, but not methysergide, had essentially similar potentiating effects to those of ketanserin. These results suggest that the 5-HT receptor that mediates prejunctional inhibition is not of the 5-HT2 type, and that ketanserin acts by suppressing the 5-HT-induced stimulatory effect, which is possibly mediated by a postjunctional 5-HT2 receptor, thus unmasking the inhibitory effect of 5-HT.

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